Anger and other strong emotion can trigger ventricular arrhythmias (VA). For example, VAs increased in the emotional weeks following the World Trade Center attacks in 2001. Further, anger can trigger polymorphic, potentially lethal VAs in patients with implantable cardioverter-defibrillators (ICDs). However, the electrophysiological mechanisms underlying the arrhythmogenic effects of emotion remain unknown. We have shown that in the laboratory setting, anger increases levels of T-wave alternans (TWA). TWA is a marker of repolarization instability which immediately precedes development of ventricular fibrillation, suggesting a mechanistic relationship. Further, TWA predicts vulnerability to sudden death and VA. However, whether anger occurring in everyday life can increase levels of TWA, a potentially arrhythmogenic phenomenon, is unknown. Based on these links between emotion and VA, a planned clinical trial, "Reducing Vulnerability to ICD Shock Treated Ventricular Arrhythmias" (Burg, 1R01HL084438-01A1) will randomize patients receiving ICDs to receive stress reduction treatment (SRT) or standard care, to determine whether 1) SRT will reduce risk of VA, 2) SRT will decrease the response of TWA to acute stress in the laboratory, and 3) SRT alters heart-rate variability, derived from 24-hour ambulatory EGG recording (holter). This ancillary study will evaluate effects of emotion on TWA in the naturalistic setting during the planned 24-hour holters. To achieve this, first, the recordings will be acquired using a new system which combines increased fidelity in data acquisition, for increased precision of TWA analysis, with built-in analytic algorithms. While subjects undergo this 24-hour holter, state-of-the-art techniques in ecological momentary assessment will measure levels of anger and other emotions in daily life, which will be correlated with simultaneously-acquired levels of TWA. The first goal of this study is to determine whether anger and anxiety in daily life will increase repolarization instability, as measured by TWA, in patients with known risk for VA and ICDs. The next goal is to examine whether effects of emotion on repolarization instability in daily life can be predicted by those in the laboratory. The final goal is to evaluate whether greater anger-induced increases in TWA during daily life correlate with subsequent VA. Determining mechanisms underlying the arrhythmogenic effects of emotion is an important step in guiding future therapeutic interventions.